角色的beta-3-adrenoceptor catecholamine-induced风头从控制和糖尿病大鼠胃底。
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Ozakca我Arioglu E,枪手,Altan VM, Ozcelikay
角色的beta-3-adrenoceptor catecholamine-induced风头从控制和糖尿病大鼠胃底。
药理学。2007;80 (4):227 - 38。Epub 2007年7月6日。
- PubMed ID
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17622774 (在PubMed]
- 文摘
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的贡献beta-adrenoceptor亚型在胃底部catecholamine-mediated放宽了从控制和链脲霉素(STZ)全身糖尿病老鼠了。孤立的器官浴研究和分子技术被用来描述beta-adrenoceptor亚型介导大鼠胃底部的放松。由nadolol Isoprenaline-mediated放松没有明显变化(β(1)- /β肾上腺素能受体拮抗剂(2);1 micromol / l),但只向右平移SR59230A (3 - (2-ethylphenoxy) 1 - [[(1) 1、2、3, 4-tetrahydronaphth-1-yl]氨基]- (2 s)丙胺草酸盐,0.1 - 1 micromol / l),选择性β肾上腺素能受体拮抗剂(3),以竞争的方式。松弛剂浓度的方式对去甲肾上腺素的反应的敌意,SR59230A (0.1 1 micromol / l),但不是通过美托洛尔(选择性β(1)肾上腺素能受体拮抗剂;0.1 - 1 micromol / l)和ici - 118551 (1 - (2, 3 - (dihydro-7-methyl-1Hinden - 4-yl)氧)3 -(1 -甲基乙基)氨基2 -丁醇盐酸,选择性β肾上腺素能受体拮抗剂(2);0.1 - 1 micromol / l)。SR59230A (1 micromol / l)向右也引起了重大转变fenoterol-induced放松而ici - 118551 (1 micromol / l)没有任何影响。选择性β(3)肾上腺素能受体激动剂,BRL37344 ([4 - (2 - [(2 - (3-chlorophenyl) 2-hydroxyethyl)氨基)丙基)苯氧基)乙酸),造成两相的放松并没有受到nadolol (1 micromol / l)。SR59230A (1 micromol / l)废除只BRL37344反应的第一阶段。 beta(1)-, beta(2)- and beta(3)-adrenoceptor mRNA expressions have been detected in a similar intensity in gastric fundus from control rats. Experimental diabetes caused a significant decrease in E(max) and pD(2) values of isoprenaline and noradrenaline. Diabetes also reduced E(max) but not pD(2) value of the first component of BRL37344-induced relaxation response. The band intensity of mRNA transcript of beta(3)-adrenoceptor was reduced in diabetics while no alteration has been found for beta(1)- and beta(2)-adrenoceptor mRNA transcripts between groups. These results show that functional beta-adrenoceptor subtype involved in catecholamine-mediated relaxations is beta(3)-adrenoceptor, and its function and mRNA expression are decreased in diabetes.